The xanthophyll cycle as an early pathogenic target to deregulate guard cells during Sclerotinia sclerotiorum infection.

Stomata not only control the important balance between gaseous fluxes and water loss, but also act as a route of invading pathogen entry into the plant. Here, the stomatal opening was observed to be induced by a necrotrophic pathogen Sclerotinia sclerotiorum at the early stages of infection. In contrast to uninfected control, the stomatal pores were still opened in S. sclerotiorum-infected regions after dark adaption. Mutation of violaxanthin de-epoxidase, a key enzyme in the xanthophyll cycle, could partially restore the S. sclerotiorum-induced stomatal opening. Further studies showed that S. sclerotiorum invasion led to a decrease in electron transport rate, but a significant increase in non-photochemical quenching (NPQ). The decay kinetics of NPQ revealed that zeaxanthin epoxidase (ZEP, also known as ABA1) was continuous deactivation in S. sclerotiorum-infected region. HPLC-MS/MS analysis showed a slight increase of jasmonate acid (JA), but a great decrease of abscisic acid (ABA) content in S. sclerotiorum-inoculated tissue. Exogenous application of ABA but not JA could rescue the abnormal stomatal opening. Together, these results suggested that the S. sclerotiorum-induced decrease of ABA biosynthesis reduced stomatal closing via dysfunction of the xanthophyll cycle during early pathogenesis.